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Article

TASK1 (K(2P)3.1) K(+) channel inhibition by endothelin-1 is mediated through Rho kinase-dependent phosphorylation.

British journal of pharmacology - 1 Mar 2012

Seyler C, Duthil-Straub E, Zitron E, Gierten J, Scholz E P, Fink R H A, Karle C A, Becker R, Katus H A, Thomas D

Abstract excerpt

BACKGROUND AND PURPOSE: TASK1 (K(2P)3.1) two-pore-domain K(+) channels contribute substantially to the resting membrane potential in human pulmonary artery smooth muscle cells (hPASMC), modulating vascular tone and diameter. The endothelin-1 (ET-1) pathway mediates vasoconstriction and is an established target of pulmonary arterial hypertension (PAH) therapy. ET-1-mediated inhibition of TASK1 currents in hPASMC...

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Share to Hypertension, Pulmonary

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Potassium Channels, Tandem Pore Domain

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Share to Receptor, Endothelin A

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Source

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Identifiers

PMID: 21838752
DOI: 10.1111/j.1476-5381.2011.01626.x
PMCID: PMC3372730

Genes

PAH

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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